Bio Categories

Posted on August 18, 2013 by MaryO
Chemical structure of cortisol.

Chemical structure of cortisol. (Photo credit: Wikipedia)

List of all the categories from Cushing’s Bios

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Mortality in Cushing’s syndrome: data from 386 patients from a single tertiary referral center

Posted on August 16, 2013 by MaryO

Source

M Yaneva, Endocrinology, Medical University, Sofia, 1341, Bulgaria.

European Journal of Endocrinology, 08/16/2013  Review Article

Yaneva MK et al. – Data on the incidence, mortality and causes of death in patients with Cushing’s syndrome (CS) are scarce, due to the rarity of CS. The aim of the study was to analyze mortality rates in CS in a large cohort of patients of all etiologies and to determine the cause of death. Patients with CS have increased mortality due to vascular events and infections.

Abstract

OBJECTIVE:

Data on the incidence, mortality and causes of death in patients with Cushing’s syndrome (CS) are scarce, due to the rarity of CS. The aim of the study was to analyze mortality rates in CS in a large cohort of patients of all etiologies and to determine the cause of death.

DESIGN:

This was a retrospective study of patients with CS, treated over a period of 45 years in the main tertiary referral center in Bulgaria.

METHODS:

386 patients with CS of all etiologies were included. The main outcome measures were the standardized mortality ratio (SMR) and the cause of death.

RESULTS:

Mean (± SD) age at diagnosis was 38±13 years; 84% of patients were women; mean follow up was 85 months (range: 0-494 months). The SMR in the CS cohort was 4.05 (95% confidence interval (CI) 2.50-5.80) (p<0.0001). The following subgroups did not have a significantly increased SMR: patients with Cushing’s disease SMR – 1.88 (95%CI 0.69-4.08), adrenal adenomas 1.67 (95%CI 0.20-6.02) and ACTH-independent bilateral adrenal hyperplasia 1.14 (95 %CI 0.21-6.34). Patients with adrenal carcinomas, ectopic CS and those with CS of undetermined etiology had significantly increased SMR: 48.00 (95%CI 30.75-71.42), 13.33 (95%CI 0.00-24.59) and 4.00 (95%CI 0.48-14.45), respectively (p<0.0001). The significant predictors for mortality were active disease at death, age, male sex, etiology of the disease, the overall duration of active disease. The major causes of death were vascular events (40%) -cardiovascular 29% and cerebrovascular 11%, followed by infections (12%).

CONCLUSIONS:

Patients with CS have increased mortality due to vascular events and infections.

Read more at MDLinx

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Cyclic Cushing’s syndrome: a clinical challenge

Posted on August 11, 2013 by MaryO
  1. J R Meinardi1,2,
  2. B H R Wolffenbuttel2 and
  3. R P F Dullaart2

+Author Affiliations


  1. 1Department of Internal Medicine, Canisius Wilhelmina Ziekenhuis, PO Box 9015, 6500 GS Nijmegen, The Netherlands and 2Department of Endocrinology, University Medical Centre Groningen, University of Groningen, PO Box 30001, 9700 RB Groningen, The Netherlands
  1. (Correspondence should be addressed to: R P F Dullaart; Email:r.p.f.dullaart@int.umcg.nl)

Abstract

Cyclic Cushing’s syndrome (CS) is a rare disorder, characterized by repeated episodes of cortisol excess interspersed by periods of normal cortisol secretion. The so-called cycles of hypercortisolism can occur regularly or irregularly with intercyclic phases ranging from days to years.

To formally diagnose cyclic CS, three peaks and two troughs of cortisol production should be demonstrated. Our review of 65 reported cases demonstrates that cyclic CS originates in 54% of cases from a pituitary corticotroph adenoma, in 26% from an ectopic ACTH-producing tumour and in about 11% from an adrenal tumour, the remainder being unclassified. The pathophysiology of cyclic CS is largely unknown.

The majority of patients with cyclic CS have clinical signs of CS, which can be either fluctuating or permanent. In a minority of patients, clinical signs of CS are absent. The fluctuating clinical picture and discrepant biochemical findings make cyclic CS extremely hard to diagnose. Clinicians should therefore be aware of this clinical entity and actively search for it in all patients with suspected CS but normal biochemistry or vice versa.

Frequent measurements of urinary cortisol or salivary cortisol levels are a reliable and convenient screening tool for suspected cyclic CS. Cortisol stimulation or suppression tests may give spurious results owing to spontaneous falls or rises in serum cortisol at the time of testing. When cyclic CS is biochemically confirmed, further imaging and laboratory studies are guided by the presence or absence of ACTH dependency. In cases of suspected ectopic ACTH production, specific biochemical testing for carcinoids or neuroendocrine tumours is required, including measurements of serotonin in platelets and/or urine, chromogranin A and calcitonin.

Read the entire article here:  http://www.scribd.com/doc/159503297/Cyclic-Cushing%E2%80%99s-syndrome-a-clinical-challenge

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Prolactin Measure Didn’t Help Localize Pituitary Adenoma

Posted on August 10, 2013 by MaryO

By: SHERRY BOSCHERT, Clinical Endocrinology News Digital Network

SAN FRANCISCO – Measurements of prolactin levels during inferior petrosal sinus sampling did not help localize pituitary adenomas in patients with Cushing’s disease in a study of 28 patients, contradicting findings from a previous study of 28 patients.

The value of prolactin measurements in tumor localization using inferior petrosal sinus sampling (IPSS) remains unclear and needs further study in a larger, prospective study, Dr. Susmeeta T. Sharma said at the Endocrine Society’s Annual Meeting. The current and previous studies were retrospective analyses.

Although IPSS has been considered the standard test in patients with ACTH-dependent Cushing’s syndrome to differentiate between ectopic ACTH secretion and Cushing’s disease, there has been controversy about its value in localizing adenomas within the pituitary gland once a biochemical diagnosis of Cushing’s disease has been made. Various studies that used an intersinus ACTH ratio of 1.4 or greater before or after corticotropin-releasing hormone (CRH) stimulation have reported success rates as low as 50% and as high as 100% for tumor location.

A previous retrospective study of 28 patients with Cushing’s disease reported that adjusting the ACTH intersinus gradient by levels of prolactin before or after CRH stimulation, and combining the prolactin-adjusted ACTH intersinus ratio, improved pituitary adenoma localization. Magnetic resonance imaging (MRI) alone correctly localized the pituitary adenoma in 17 patients (61%), a prolactin-adjusted ACTH intersinus ratio of at least 1.4 improved the localization rate to 21 patients (75%), and combining MRI and the prolactin-adjusted ACTH intersinus ratio improved localization further to 23 patients, or 82% (Clin. Endocrinol. 2012;77:268-74).

The findings inspired the current retrospective study. The investigators looked at prolactin levels measured in stored petrosal and peripheral venous samples at baseline and at the time of peak ACTH levels after CRH stimulation for 28 patients with Cushing’s disease and ACTH-positive pituitary adenomas who underwent IPSS in 2007-2013. The investigators calculated prolactin-adjusted values by dividing each ACTH value by the concomitant ipsilateral prolactin value. They used an intersinus ACTH ratio of 1.4 or greater to predict tumor location.

At surgery, 26 patients had a single lateral tumor (meaning its epicenter was not in the midline), 1 patient had a central microadenoma, and 1 patient had a macroadenoma, reported Dr. Sharma of the National Institute of Child Health and Human Development, Bethesda, Md.

MRI findings accurately identified the location of 21 of the 26 lateral tumors (81%), compared with accurate localization in 18 patients using either the unadjusted ACTH intersinus ratio or the prolactin-adjusted ACTH intersinus ratio (69% for each), she said.

Incorrect tumor localization occurred with one patient using MRI alone and seven patients using either ratio. In four patients whose tumors could not be localized by MRI, the uncorrected and prolactin-adjusted ratios localized one tumor correctly and three tumors incorrectly. Only MRI correctly localized the one central microadenoma.

“We did not find any difference in localization rates by measurement of prolactin during IPSS,” she said. The small size of the study and its retrospective design invite further research in a more robust study.

Dr. Sharma reported having no financial disclosures.

From Clinical Endocrinology News

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What is the Best Approach to Suspected Cyclical Cushing Syndrome?

Posted on August 2, 2013 by MaryO

Strategies for Managing Cushing’s Syndrome With Variable Laboratory Data

Brew Atkinson, Karen R. Mullan

Disclosures

Clin Endocrinol. 2011;75(1):27-30.

 

Abstract

Cyclical Cushing’s syndrome is a pattern of hypercortisolism in which the biochemistry of cortisol production fluctuates rhythmically. This syndrome is often associated with fluctuating symptoms and signs. It is now being increasingly recognized. The phenomenon is important because it can, if not recognized, lead to errors in diagnosis and differential diagnosis of the syndrome and in assessment of therapeutic outcomes. The techniques and criteria, protocols and dynamic biochemical tools to detect cycling in patients with hypercortisolism are discussed as are the strategies for diagnosing and managing this important subgroup of patients with hypercortisolism.

Introduction

Cyclical Cushing’s syndrome (CS) is a pattern in hypercortisolism in which the biochemistry of cortisol production fluctuates rhythmically. This can also be associated with fluctuating symptoms and signs. This type of case was initially thought to be rare. However, it has recently been recognized as occurring much more frequently. The phenomenon is important because, if not recognized, it can lead to errors in diagnosis and differential diagnosis of the syndrome and in assessment of therapeutic outcomes. All of these can have very serious clinical consequences.

As a result of reading this article, it is hoped that readers will be better able to consider more carefully the risks associated with too wide a diagnostic trawl for the diagnosis of CS and the associated chances of finding some abnormality of steroid biochemistry.

In cases where the diagnosis is being strongly considered, the risks of not considering episodic secretion when laboratory results are discordant are discussed. Readers should be able to plan strategies to assess for variable and cyclical secretion and to use these in diagnosis, differential diagnosis and treatment assessments.

Read more here: What is the best approach to suspected cyclical Cushing syndrome?

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